Unraveling the roles of sphingolipids in plant innate immunity
Iwate Biotechnology Research Center, Kitakami, Iwate, JapanPlant signaling & behavior 06/2009; 4(6):536-8. DOI: 10.4161/psb.4.6.8583
It has long been known that fungal pathogens like Fusarium and Alternaria spp. produce toxins (mycotoxin) to kill plant cells. These mycotoxins have been shown to perturb the plant sphingolipid biosynthesis pathway, resulting in the necrotic cell death of plant cells. A recent study by Shi et al.1 revealed that an increase in the amount of cellular sphingoid bases triggers plant programmed cell death (PCD) through accumulation of reactive oxygen species (ROS). These studies point to the importance of sphingolipids in the regulation of plant cell in disease development as well as in defense responses. In the latest report,2 we showed that serine palmitoyltransferase (SPT), the key enzyme of sphingolipid biosynthesis, regulates not only plant cell death but also defense response against a non-host pathogen, soliciting further studies to elucidate the roles of sphingolipids in plant innate immunity.
Full-textDOI: · Available from: Ryohei Terauchi, Oct 07, 2015
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ABSTRACT: Sphingolipids play an important role in signal transduction pathways that regulate physiological functions and stress responses in eukaryotes. In plants, recent evidence suggests that their metabolic precursors, the long-chain bases (LCBs) act as bioactive molecules in the immune response. Interestingly, the virulence of two unrelated necrotrophic fungi, Fusarium verticillioides and Alternaria alternata, which are pathogens of maize and tomato plants, respectively, depends on the production of sphinganine-analog mycotoxins (SAMs). These metabolites inhibit de novo synthesis of sphingolipids in their hosts causing accumulation of LCBs, which are key regulators of programmed cell death. Therefore, to gain more insight into the role of sphingolipids in plant immunity against SAM-producing necrotrophic fungi, we disrupted sphingolipid metabolism in Nicotiana benthamiana through virus-induced gene silencing (VIGS) of the serine palmitoyltransfersase (SPT). This enzyme catalyzes the first reaction in LCB synthesis. VIGS of SPT profoundly affected N. benthamiana development as well as LCB composition of sphingolipids. While total levels of phytosphingosine decreased, sphinganine and sphingosine levels increased in SPT-silenced plants, compared with control plants. Plant immunity was also affected as silenced plants accumulated salicylic acid (SA), constitutively expressed the SA-inducible NbPR-1 gene and showed increased susceptibility to the necrotroph A. alternata f. sp. lycopersici. In contrast, expression of NbPR-2 and NbPR-3 genes was delayed in silenced plants upon fungal infection. Our results strongly suggest that LCBs modulate the SA-dependent responses and provide a working model of the potential role of SAMs from necrotrophic fungi to disrupt the plant host response to foster colonization.Planta 09/2012; 237(1). DOI:10.1007/s00425-012-1758-z · 3.26 Impact Factor